Background Collagen type I is one of the major deposits in thickening of the reticular basement membrane of asthma.
Objective and Methods In this study, we assessed turnover of collagen type I in asthma by measuring procollagen type I C-terminal peptide (PICP) and collagen type I C-terminal telopeptide (ICTP) in induced sputum.
Results PICP but not ICTP was found to be significantly higher in asthma subjects than in normal volunteers (P < 0.05). In asthma, PICP was inversely correlated with %FEV1.0 (r = −0.539), and its levels significantly increased upon exacerbation (P < 0.05), indicating that collagen synthesis increases during asthma exacerbation. Additionally, PICP was found to significantly correlate with eosinophil counts in sputum (r = 0.539), indicating that eosinophils stimulate collagen turnover. Because eosinophils can produce TGF-β, a potent stimulator of collagen synthesis, we immunocytochemically examined TGF-β-positive cells in sputum. TGF-β-positive cells significantly correlated with eosinophil counts (r = 0.811) and PICP (r = 0.569), suggesting that TGF-β released from eosinophils is involved in collagen synthesis.
Conclusions The results of the present study suggest that collagen synthesis is stimulated in asthmatic airways by eosinophils through TGF-β, while collagen degradation is not, and that PICP in sputum can act as a new marker for airway inflammation in asthma.
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